Fig. 5
CaMKIIα neurons in the LPBN mediate the disruption of acute inflammatory pain on 3CSRTT performance. A–J The effect of chemogenetic inhibition of CaMKIIα neurons in the LPBN on acute inflammatory pain-induced 3CSRTT performance impairment. A Schematic of bilateral LPBN stereotaxic injection of AAV-CaMKIIα-mCherry or AAV-CaMKIIα-hM4Di-mCherry in naive mice. B Representative image of the restricted expression of AAV-CaMKIIα-hM4Di-mCherry in the bilateral LPBN. Scale bar, 800 μm. C Higher magnifications of the specified region in (B). Scale bar, 200 μm. D Experimental design. Mice were i.p. injected with CNO (2.5 mg/kg) 30 min before formalin intraplantar injection, and 3CSRTT was performed immediately after formalin injection for 60 min. E, F Correct (E) and omission (F) over the 60-min testing period in CaMKIIαmCherry and CaMKIIαhM4Di mice. Data points are displayed in 5-min time bins. G, H Correct response latency (G) and reward latency (H) in CaMKIIαmCherry and CaMKIIαhM4Di mice. I, J Correct (I) and omission (J) in phases 1 and 2 in CaMKIIαmCherry and CaMKIIαhM4Di mice (n = 7 mice per group). K–Q The effect of chemogenetic activation of CaMKIIα neurons in the LPBN on 3CSRTT performance. K Schematic of bilateral LPBN stereotaxic injection of AAV-CaMKIIα-mCherry or AAV-CaMKIIα-hM3Dq-mCherry in naive mice. L Representative image of the restricted expression of AAV-CaMKIIα-hM3Dq-mCherry in LPBN and CNO-evoked c-Fos expression in virally labelled neurons. M Experimental design. 3CSRTT (50 trials) was performed 30 min after saline i.p. injection on the first day. The next day, 3CSRTT was performed 30 min after CNO i.p. injection. N–Q Correct (N), omission (O), incorrect (P), and premature (Q) in the 3CSRTT in CaMKIIαmCherry and CaMKIIαhM3Dq mice (n = 7 mice per group). Data are mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. Two-way ANOVA followed by the Sidak’s multiple comparisons test in E, F and N–Q. Two-tailed unpaired t test in G–J